Polymorphic light eruption (PLE) is a photodermatosis with an extremely high prevalence,
particularly among young women (up to 20%). The disease is characterized through itchy skin
lesions on sun-exposed body sites occurring after sun exposure mostly in spring and early
summer. Its etiopathogenesis is unknown but resistance to ultraviolet radiation (UVR)-induced
immunosuppression with subsequent immune reactions against skin photoneoantigens has been
suggested.
The phenomenon of UVR-induced immunosuppression (suppression of CHS) has been well known for
many years. Recent findings showed that regulatory T cells (CD4+CD25+FoxP3+) (Tregs), a
subset of T helper cells, are crucial in UVR-induced immunosuppression. However, the
requirements for the maintenance of peripheral CD4+CD25+ T cells, important in suppression of
immune responses, are still incompletely understood. Recent work suggests that cutaneous
RANKL might be the physiologic missing link that couples UVR to immunosuppression. Epidermal
RANKL, expressed in keratinocytes of inflamed skin due to e.g. UVR exposure was shown to
control the number of Tregs via activation of dendritic cells, hereby mediating UVR-induced
immunosuppression (e.g. suppression of allergic contact hypersensitivity responses). In
addition to the suppression of local cutaneous hyperallergic responses, the development of
systemic autoimmunity is suppressed. A strong inducer of RANKL expression and of Tregs is
vitamin D3 that has been reported to have immunosuppressive effects. Interestingly, patients
with autoimmune disorders (e.g. lupus erythematosus) may exhibit reduced vitamin D3 blood
levels.
This randomized, double blinded left-right body side experimental comparison study was
designed to assess the preventive effect of the vitamin D3 analogue calcipotriol in patients
with PLE. The hypothesis is tested that treatment with a calcipotriol-containing cream can
prevent the UVR-induced development of PLE skin lesions. Better insight into the pathogenesis
of PLE may give clues to develop new therapeutic strategies.